Valvular Heart Disease: Changing Concepts in
Disease Management
Cardiovascular Magnetic Resonance Imaging for Valvular
Heart Disease
Technique and Validation
Peter J. Cawley, MD; Jeffrey H. Maki, MD, PhD; Catherine M. Otto, MD
O ver the last half century, clinicians have employed several
means to advance our knowledge of the causes and
consequences of valvular heart disease. Invasive cardiac cathe-
terization provided valuable information about hemodynamics,
2-dimensional (2D) echocardiography (echo) allowed direct
visualization of the valvular apparatus and cardiac chambers,
and Doppler echocardiography afforded a noninvasive tool for
assessing hemodynamics and disease severity.
Echocardiography is now the standard tool for initial
assessment and longitudinal evaluation of patients with val-
vular heart disease; however, echocardiography is limited in
patients with poor acoustic windows and may be more
operator dependent than other modalities, particularly for
quantitation of disease severity. In the last 20 years, cardio-
vascular magnetic resonance (CMR) has emerged as an
alternative noninvasive modality without ionizing radiation
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that is applicable to patients with valvular heart disease. CMR
provides images of valve anatomy and allows quantitative
evaluation of stenosis and regurgitation. CMR can also
discern the consequences of the valvular lesion, including the
effects of ventricular volume or pressure overload and alter-
ations in systolic function. The purpose of the present review
is to summarize the general principles of CMR and validate
CMR as a tool for evaluation of valvular heart disease.
General Principles
CMR uses a variety of pulse sequences to assess valvular
heart disease (Table 1). A pulse sequence is a combination of
transmitted radiofrequency pulses and magnetic gradients in
the presence of a strong external magnetic field, from which
a series of received radiofrequency pulses or “echoes” are
obtained and processed into an image.1,2
Anatomy
CMR has the potential to visualize all parts of the valve
(leaflets, chordae tendineae, and papillary muscles) through-
out the entire cardiac cycle. Congenitally abnormal valve
leaflets (bicuspid), aberrant papillary muscles or aberrant
From the Division of Cardiology (P.J.C., C.M.O.), Department of Medicine, and Department of Radiology (J.H.M.), University of Washington, Seattle, Wash.
Guest Editor for this article was James E. Udelson, MD.
Correspondence to Peter J. Cawley, MD, 1959 NE Pacific St, Box 356422, Division of Cardiology, Seattle, WA 98195-6422. E-mail pcawley@u.
washington.edu
(Circulation. 2009;119:468-478.)
© 2009 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.org
468
chordal attachments (parachute mitral valve), leaflet thicken-
ing, presence and extent of calcification, leaflet redundancy
and prolapse, and commissural fusion are all anatomic
descriptions that have been reported by CMR. However,
2-dimensional (2D) echocardiography is superior for imaging
structures that are thin and highly mobile owing to its greater
temporal resolution and the absence of partial volume effects.
Although 2D echocardiography remains the primary ap-
proach for visualization of valve anatomy, CMR is a reason-
able alternative if ultrasound windows are poor.
In addition, CMR can provide visualization of valve
masses such as vegetations, thrombi, or tumors, including
attachment site and mobility.3– 6 For masses of sufficient size,
tissue characterization may be helpful when the origin of the
mass is unknown.4,6 However, the minimum size of the mass
needed for detection by CMR has not been described, and
sensitivity and specificity compared with 2D echocardiogra-
phy have not been evaluated.
The steady-state free precession (SSFP) cine pulse se-
quence is the most widely used CMR pulse sequence for
assessing valve anatomy and motion (Figures 1 and 2). This
pulse sequence has excellent blood-to-myocardium contrast
and a high intrinsic signal-to-noise ratio and has largely
replaced gradient echo as the preferred pulse sequence for
cine imaging of valve anatomy. SSFP produces a 2D image in
any prescribed plane having multiple phases (frames)
throughout the cardiac cycle, with a typical temporal resolu-
tion of 25 to 50 ms. To produce an SSFP cine image
throughout all of systole and diastole, image acquisition is
gated to the ECG and occurs over several cardiac cycles,
easily obtained in a single breath hold (6 to 12 seconds).
Non-cine pulse sequences such as turbo spin echo (T1
weighted, T2 weighted, fat saturation) and segmented inver-
sion recovery gradient recalled echo pulse sequences may aid
in tissue characterization of valve masses.4,6
Velocity
SSFP and gradient echo cine pulse sequences can visualize
flow turbulence (Figure 3) on the basis of loss of signal
DOI: 10.1161/CIRCULATIONAHA.107.742486
 Cawley et al
Table 1. CMR Pulse Sequences for Valvular Heart Disease
Pulse Sequence Indication
SSFP cine Valve anatomy and motion
Ventricular volumes and function
Gradient echo cine Valve anatomy and motion
Turbulent flow
Phase contrast Velocity
Forward and regurgitant
volumes
Turbo spin echo (T1, T2, with or Valve mass characterization
without fat saturation)
Segmented inversion recovery Valve mass characterization
gradient echo
(signal void) due to the dephasing of moving protons. This
approach can help show the location of “jets” and optimize
the location of velocity sampling. Although SSFP provides
improved visualization of valve anatomy, it is less sensi-
tive for depicting flow disturbances. This can lead to
underestimation or the overlooking of a regurgitant jet.
Gradient echo cine pulse sequences, on the other hand, are
more sensitive for the detection and sizing of regurgitant
jets. With gradient echo sequences, the sensitivity for
detecting dephasing (eg, valve regurgitation) is a function
of the echo time: the longer the echo time, the larger and
more pronounced the regurgitant jet.7
Phase-contrast pulse sequences (other names include
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velocity-encoded cine, Q flow, or velocity mapping) are used
for velocity measurements and are based on the accumulated
phase of moving protons. In this pulse sequence, bipolar
gradients oriented in the expected direction of blood flow are
applied to each frame of the imaging slice of interest to
induce phase shifts.8 Phase refers to the angular position of an
individual proton’s spin vector with respect to a frame of
reference. Stationary objects within this slice have a net phase
of zero, because all phase induced by the first lobe of the
bipolar gradient is reversed by the second lobe. Moving
objects (blood) gain a net phase depending on the direction of
blood flow, and this net phase (or phase shift) is proportional
CMR for Valve Disease: Technique and Validation 469
to the velocity of blood. This net phase can be displayed as a
phase map with differences in signal intensity representing
different velocities (Figure 4). Pixels depicting flow in the
phase-encoding direction appear bright (Figure 4A), and flow
opposite to the phase-encoding direction appears dark (Figure
4B). Objects with a phase shift of zero (stationary) are gray or
speckled, as can be seen in the lungs or chest wall.
Velocity mapping requires that the appropriate maximum
velocity be programmed into the pulse sequence. Aliasing
occurs if the angular phase shift is ⬎180°, and the velocity
within that pixel is then misregistered. This occurs if the
programmed maximum velocity is less than the sampled
velocities of blood flow in the imaging slice. The closer the
programmed maximum velocity is to the maximum velocity
present, the greater the sensitivity and accuracy of this
technique to detect lower velocities within the region of
interest.
Velocity mapping produces 2 sets of images: magnitude
image and phase velocity maps (Figure 4). The magnitude
image is used for anatomic orientation of the imaging slice
and to identify the boundaries of the vessel imaged. Blood has
an increased signal, whereas turbulent flow is depicted with
signal loss within the magnitude image. The phase map
encodes the velocities within each pixel. Using both images,
a region of interest can be traced on each time frame of the
data set. The region of interest must be drawn for each frame
of the cardiac cycle carefully because of movement and
deformation of the vessel. Within each region of interest, the
peak instantaneous velocity (Vmax) for each time frame can
also be obtained. With the simplified Bernoulli equation
(4V2max), the peak instantaneous gradient can be estimated by
substituting in the peak instantaneous velocity. Mean pressure
gradients are obtained by averaging all of the instantaneous
velocities over systole. With flow phantoms, phase velocity
mapping has been shown to accurately measure velocities
over 5 m/s.9
Flow Volume
Velocity maps can also be used to determine flow volume
throughout the cardiac cycle. With the same magnitude and
Figure 1. SSFP images of abnormal
mitral and aortic valves with the abnor-
mal valve leaflets (A) closed and (B) at
maximal opening. Rheumatic mitral ste-
nosis is shown in the 3-chamber and
short-axis image plane. Note significant
thickening and calcification of both the
mitral valve leaflets and chordae tendi-
neae, along with chordal fusion, as well
as severe left atrial enlargement. At max-
imal opening of the mitral valve leaflets,
the signal void seen within the left ventri-
cle represents turbulent diastolic filling of
the left ventricle (arrow). A bicuspid aor-
tic valve with significant aortic stenosis
is shown in a short-axis image plane.
MR images courtesy of Raymond J. Kim,
MD, Duke Cardiovascular Magnetic Res-
onance Center, Durham, NC.
 470 Circulation January 27, 2009

Figure 2. A, Systolic frame of a 3-chamber SSFP image of myxomatous mitral valve disease. Note that the aortic valve leaflets are
opened. The anterior and posterior mitral valve leaflets are redundant. B, Two phases later in systole, significant prolapse of both the
anterior and posterior mitral valve leaflets occurs. The dashed arrow represents signal void from mitral regurgitation. C, One phase later
in systole, mitral regurgitation worsens (dashed arrow). This is an example of late systolic mitral regurgitation. This patient had a mitral
regurgitant fraction of 40%. Involvement of all segments of both mitral valve leaflets suggests a low likelihood of valve repairability. Ao
indicates aorta; LV, left ventricle; and PM, papillary muscle.

phase velocity maps, a region of interest is traced around the
vessel lumen to determine the area of the vessel, frame by
frame. By multiplying the velocity (cm/s) of each pixel by the
area (cm2) of the region of interest, the instantaneous flow
volume (cm3/s) is obtained for each frame of the cardiac
cycle. The instantaneous flow volume of each frame (y-axis)
can be plotted against the time of the cardiac cycle (x-axis) to
show bulk flow as it relates to the cardiac cycle (Figure 5).
When the area under the curve is integrated for systole and
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mitral regurgitation, in vivo stroke volume by the Fick
principle and by thermodilution, in vivo stroke-volume mea-
surements by Doppler, and in vitro stroke-volume measure-
ments within continual and pulsatile flow phantoms.10 –14
Potential Pitfalls for Phase-Contrast Imaging
Although the “in-plane” pixel size for phase-contrast imaging
may be on the order of 1.5 to 2.0 mm, the slice thickness
(volume of tissue) is typically 6 to 8 mm. Thus, vena
contracta velocities may be underestimated owing to averag-

diastole, forward and regurgitant volumes can be generated.
Stroke-volume measurements by velocity mapping in the
ascending aorta have been shown to have a strong correlation
to in vivo stroke-volume measurements by cine CMR pulse
sequences of the left ventricle in subjects without significant
ing of flow velocities from inside and outside the actual vena
contracta (partial volume averaging). In these circumstances,
velocity measurements for each pixel may be lower than
actual velocities. Furthermore, the smaller the structure of
interest, the fewer pixels are fully within this region, which

Figure 3. A, Three-chamber SSFP image

of the left ventricular outflow tract. In
systole, the arrow demonstrates flow
turbulence (signal void) that begins at
the level of the aortic valve leaflets. This
patient has an antegrade velocity of 3.1
m/s. In diastole, the arrow demonstrates
flow turbulence (signal void) that begins
at the level of the aortic valve, consistent
with central aortic regurgitation. This
patient had a regurgitant fraction of
39%. B, SSFP image of the right ventric-
ular outflow tract in a patient with
repaired tetralogy of Fallot. Essentially
no pulmonic valve leaflets remain, and
pulmonic regurgitation is wide open
(arrows demonstrate signal void), with a
regurgitant fraction of 55%. LA indicates
left atrium; LV, left ventricle; RA, right
atrium; and RV, right ventricle.
 Cawley et al
amplifies the effects of partial volume averaging. Limited
temporal resolution reduces the accuracy of CMR velocity
measurements. Lower frame rates may not be able to capture
high velocities of short duration, which results in underesti-
mation of peak velocities. In addition, it is very important for
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the imaging slice to be oriented perpendicular to the flow of
blood. If the angle of intercept is not 90°, an increased
likelihood exists of inaccurate velocity measurements.
Ventricular Volumes and Function
Left ventricular volume assessment by CMR has been per-
formed in several ways. In 1 method, the same formula used
for biplane left ventriculography can be applied to the 2- and
4-chamber CMR views.15 However, these types of formulas
depend on left ventricular geometric assumptions that may
not apply to any individual patient. Left and right ventricular
volume assessment is optimally performed with multislice 2D
SSFP cine imaging covering both ventricles. A parallel stack
of serial images (short-axis or 4-chamber) is acquired from
Figure 5. Area graph of the data obtained from the velocity
maps in Figure 4. This demonstrates a pulmonic regurgitant
fraction of 52%.
CMR for Valve Disease: Technique and Validation 471
Figure 4. Systolic (A) and diastolic (B)
quantitative flow images through the pul-
monary artery. The magnitude image
details the anatomy, contour, and shape
of the pulmonary artery (arrow). On the
phase velocity map, flow in the phase-
encoding direction is represented by
bright signal (systole) within the artery
lumen, and flow opposite to the phase-
encoding direction is represented by
dark signal (diastole). Gray (*) or speck-
led (§) signal represents stationary
objects such as air and the chest wall,
respectively. Notice the shape of the
pulmonary artery changes slightly in di-
astole, best demonstrated on the magni-
tude image. The dark pulmonary artery
signal on the velocity map represents
pulmonic valve regurgitation.
base to apex of the left ventricle (Figure 6) with a 6- to 8-mm
slice thickness. Most commonly, an imaging “gap” of 2 to
4 mm is used to balance the accurate assessment of ventric-
ular volumes against excessive prolongation of total scan
time. Volume for each image plane is calculated as the area of
the endocardial tracing multiplied by the addition of the
image slice thickness and interslice gap. End-diastolic and
-systolic volumes are calculated by summing all slices, which
allows for calculation of stroke volume, cardiac output, and
ejection fraction with standard equations.
The accuracy of CMR-calculated LV volumes has been
validated both in vitro and in vivo. In vitro, a close correlation
has been shown between CMR ventricular volumes and
fluid-filled phantoms, wax casts of porcine ventricular cavi-
ties, latex casts of cadaveric hearts, and dynamic (pulsatile-
flow) phantoms.16,17 In vivo, a close correlation between left
and right ventricular stroke volumes has been shown in
normal subjects with excellent reproducibility.16,18 Right
ventricular volumes have also been validated in vitro to casts
of cadaveric hearts.19
Areas of delayed gadolinium enhancement of the left
ventricular myocardium correlate histopathologically with
infarction20 but have also been described in patients with
hypertrophic, dilated, and infiltrative cardiomyopathies. Sev-
eral patterns of delayed gadolinium enhancement have been
reported in adults with severe aortic stenosis,21,22 although the
clinical implications of these findings in terms of prognosis
and timing of intervention have not been fully elucidated.
Evaluation of Valve Stenosis
Standard measures of stenosis severity are used for CMR:
peak antegrade velocity, pressure gradient, and valve area.
 472 Circulation January 27, 2009

Figure 6. A, Four-chamber SSFP image

at end diastole. The lines represent the
imaging locations of serial short-axis
images taken to assess ventricular vol-
umes. B, A single representative short-
axis SSFP image of the mid ventricle at
end diastole and end systole, respec-
tively, with the endocardial borders
traced to obtain left ventricular volume.
The difference between end-diastolic
and end-systolic area is multiplied by the
sum of the slice thickness and interslice
gap to calculate stroke volume.

Peak Antegrade Velocity and Pressure Gradient
Validation studies in human subjects have been published as
early as the 1990s showing that antegrade velocity correlates
well with continuous-wave Doppler echocardiography in
adults with aortic stenosis. A trend can be identified for CMR
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to underestimate the peak velocity, most likely because of
partial volume averaging within the vena contracta (Table
2).23–31 In patients with mitral stenosis, inflow velocities as
assessed by Doppler echocardiography and CMR phase-
contrast imaging correlate well (Table 3).23,32–37

Table 2. Select Studies Validating Indices of Aortic Stenosis by CMR

Reference Mean Difference⫾1 SD CMR Reproducibility*:
First Author (Year) Principle Standard n r (CMR⫺Echo) Mean Difference⫾1 SD
Velocity/gradients
Kilner23 (1993) V̇max TTE 26† 䡠䡠䡠 ⫺0.10⫾0.46 m/s 0.11⫾0.29 m/s‡
Eichenberger24 (1993) peak ⌬P TTE 15 䡠䡠䡠 2.6⫾13.3 mm Hg 䡠䡠䡠
mean ⌬P 0.96 ⫺0.6⫾8.5 mm Hg
Sondergaard25 (1993) V̇max TTE 12 䡠䡠䡠 ⫺0.88⫾0.91 m/s 䡠䡠䡠
Caruthers26 (2003) peak ⌬P TTE 24 0.82 䡠䡠䡠 r⫽0.94§
mean ⌬P 0.87
Physiological valve area
Caruthers26 (2003) continuity equation TTE 24 0.83 䡠䡠䡠 r⫽0.94§
Anatomic valve area
John27 (2003) planimetry㛳 TEE 40 0.96 0.02⫾0.08 cm2¶ 0.07⫾0.06 cm2‡
0.05⫾0.04 cm2#
Kupfahl28 (2004) planimetry TEE 32 䡠䡠䡠 0.02⫾0.21 cm2 0.03⫾0.05 cm2‡
⫺0.02⫾0.06 cm2#
Debl29 (2005) planimetry TEE 25 0.86 0.13⫾0.16 cm2¶ 䡠䡠䡠
Reant30 (2006) planimetry TEE 39 0.58 0.01⫾0.14 cm2 0.03⫾0.14 cm2‡
(Echo⫺CMR) 0.02⫾0.07 cm2#
Schlosser31 (2007) planimetry TEE 32 0.82 0.15⫾0.13 cm2 0.75**‡
n Indicates sample size; TTE, transthoracic echocardiography; peak ⌬P, peak pressure gradiant; mean ⌬P, mean pressure gradient; and TEE, transesophageal
echocardiography.
If not stated in the publication, statistics were calculated from the data provided in the manuscript. If this was not performed or data were not provided, a designation of
“not available” (...) was given.
*Reported as mean difference⫾1 SD; if not available, the statistical test provided by the author is stated.
†This analysis included 17 aortic stenosis and 9 mitral stenosis measurements.
‡Interobserver reproducibility.
§Interstudy reproducibility.
㛳Cine MRI pulse sequence was gradient echo; the other planimetry studies used an SSFP cine sequence.
¶Mean absolute difference.
#Intraobserver reproducibility.
**Kendall’s statistic.
 Cawley et al CMR for Valve Disease: Technique and Validation 473

Table 3. Select Studies Validating Indices of Mitral Stenosis by CMR

Mean Difference⫾1 SD CMR Reproducibility*:
First Author (Year) CMR Method Reference Standard: Method n r (CMR⫺Other Modality) Mean Difference⫾1 SD
Velocity/gradients
Mohiaddin32 (1991) V̇max TTE: V̇max 5 䡠䡠䡠 ⫺0.12⫾0.27 m/s 䡠䡠䡠
Kilner23 (1993) V̇max TTE: V̇max 26† 䡠䡠䡠 0.10⫾0.46 m/s 0.11⫹0.29 m/s‡
Hartiala33 (1993) E velocity TTE: E velocity 10§ 0.68 䡠䡠䡠 0.16%‡§
A velocity TTE: A velocity 0.83 0.68%‡§
Heidenreich34 (1995) peak ⌬P TTE: peak ⌬P 14 0.89 Vmax: 0.38⫾0.2 m/s 0.001 m/s‡
mean ⌬P TTE: mean ⌬P 0.95 (Echo⫺CMR)
Valve areas
Lin35 (2004) T1⁄2, T2 TTE: T1⁄2 17 0.86 0.5⫾0.59 cm2 r⫽0.96‡
36
Djavidani (2005) planimetry TTE: T ⁄
12 22 0.81 0.13⫾0.24 cm2㛳 0.03⫾0.01 cm2‡¶
catheterization: Gorlin 17 0.89 0.08⫾0.22 cm2㛳 0.04⫾0.02 cm2#¶
Djavidani37 (2006) planimetry** TTE: T1⁄2 13 0.98 0.03⫾0.09 cm2㛳 䡠䡠䡠
catheterization: Gorlin 13 0.95 0.13⫾0.15 cm2㛳
n Indicates sample size; TTE, transthoracic echocardiography; and T1⁄2, pressure half time.
If not stated in the publication, statistics were calculated from the data provided in the manuscript. If this was not performed or data were not provided, a designation of
“not available” (...) was given.
*Reported as mean difference⫾1 SD; if not available, the statistical test provided by the author is stated.
†This analysis included 17 aortic stenosis and 9 mitral valve measurements.
‡Interobserver reproducibility.
#Intraobserver reproducibility.
§Normal volunteers only. Interobserver reproducibility: (observer 1⫺observer 2)/(mean of observer 1 and observer 2) and expressed in percentages.
㛳Mean absolute difference.
¶Coefficient of variation.
**Includes 5 patients before and after balloon valvuloplasty.
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Valve Area
In aortic stenosis, the valve area can be defined in 2 different
ways: anatomic valve area and physiological valve area. An
anatomic valve area is defined as the planimetered area of
maximal opening of the aortic valve leaflets. CMR planim-
etry for the assessment of anatomic aortic valve area is based
on direct visualization of the valve orifice, made possible by
the excellent blood-to-myocardium contrast and high signal-
to-noise ratio provided by SSFP (Table 2).23–31 SSFP planim-
etry has been shown to correlate better with planimetry using

Table 4. Select Studies Validating Methods of Aortic Regurgitant Severity by CMR

First Author (Year) CMR Method Reference Standard: Method n r CMR Reproducibility
45
Globits (1990) spin echo cine*: RF with catheterization: RF 20 0.91 interobserver mean variation
biventricular volumes in RVSV⫽7 mL, LVSV⫽7.3
mL
Aurigemma46 (1991) gradient echo cine: regurgitant TTE: regurgitant jet area by 13 0.88 䡠䡠䡠
jet area by signal void color Doppler
Dulce47 (1992) velocity mapping: RV, RF gradient echo cine†: RV and 10 RV 0.975; RF 0.991 interstudy: RV r⫽0.977, RF
RF with biventricular r⫽0.986; interobserver: RV
volumes r⫽0.99, RF r⫽0.99
Honda48 (1993) velocity mapping: RF TTE: regurgitant area by 26 interobserver r⫽0.956
color Doppler
catheterization: angiographic 9 䡠䡠䡠 intraobserver r⫽0.998
grade by aortogram
Sondergaard49 (1993) velocity mapping: RV catheterization: angiographic 9 0.8
grade by aortogram
Ley50 (2007) velocity mapping: RF TTE‡: pulsed Doppler RF 30 0.68 䡠䡠䡠
n Indicates sample size; RF, regurgitant fraction; interobserver, interobserver reproducibility; interstudy, interstudy reproducibility; RVSV, right ventricular stroke
volume; LVSV, left ventricular stroke volume; TTE, transthoracic echocardiography; RV, regurgitant volume; and Intraobserver, intraobserver reproducibility.
If not stated in the publication, statistics were calculated from the data provided in the manuscript. If this was not performed or data were not provided, a designation of
“not available” (...) was given.
*Regurgitant fraction (%)⫽(LVSV⫺RVSV)/LVSV⫻100.
†RV⫽LVSV⫺RVSV; RF (%)⫽(LVSV⫺RVSV)/LVSV⫻100.
‡RF (%)⫽total stroke volume⫺forward stroke volume/total stroke volume⫻100.
 474 Circulation January 27, 2009

Table 5. Select Studies Validating Methods of Mitral Regurgitant Severity by CMR

CMR Reproducibility*:
First Author (Year) CMR Method Reference Standard: Method n r Mean Difference⫾1 SD
Sechtem51 (1988) gradient echo cine†: RF with biventricular TTE‡: pulsed Doppler RF 8 0.9 r⫽0.96§, r⫽0.99㛳
volumes
Nishimura52 (1989) gradient echo cine: regurgitant jet area TTE: jet area 20 0.71 r⫽0.96§
and length by signal void TTE: jet length 0.74
Glogar53 (1989) spin echo cine¶: RF with biventricular catheterization: RF 13 0.84 䡠䡠䡠
volumes
gradient echo cine: regurgitant jet area catheterization: angiographic 20 0.73
by signal void grade by aortogram
TTE: jet area 26 0.77
54
Aurigemma (1990) gradient echo cine: regurgitant jet area TTE: jet area 20 0.74 䡠䡠䡠
by signal void
Globits45 (1990) spin echo cine#: RF with biventricular catheterization: RF 26 0.67 RVSV 7 mL§**; LVSV
volumes 7.3 mL§**
Fujita55 (1994) velocity mapping: (LV mitral inflow⫺Ao TTE: jet area 29 RV 0.74 RV r⫽0.99§
outflow)
RV and RF RF 0.87 RF r⫽0.98§
controls (no MR) 0.96
Hundley56 (1995) velocity mapping††: (LV cine and aortic catheterization: RV index 23 0.97 FSV 3⫾3%§
phase contrast)
RV index and RF RF 0.96 TSV 9⫾7%§
RF 10⫾9%§
Kizilbash57 (1998) velocity mapping‡‡: (LV cine and aortic TTE:
phase contrast) RF pulsed Doppler RV 22 0.92 䡠䡠䡠
pulsed Doppler RF 0.82
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Kon58 (200$0) velocity mapping††: (LV cine and aortic gradient echo cine: RF with 28 䡠䡠䡠 VM 0.6⫾4.8%㛳
phase contrast) RF biventricular volumes VM ⫺2⫾7.7%§
GEC ⫺2⫾6.7%㛳
GEC 0.4⫾8.8%§
n Indicates sample size; RF, regurgitant fraction; TTE, transthoracic echo; RVSV, right ventricular stroke volume; LVSV, left ventricular stroke volume; LV, left
ventricular; Ao, aortic; RV, regurgitant volume; MR, magnetic resonance; FSV, forward stroke volume; TSV, total stroke volume; VM, velocity mapping; and GEC,
gradient cine.
If not stated in the publication, statistics were calculated from the data provided in the manuscript. If this was not performed or data were not provided, a designation of
“not available” (...) was given.
*Reported as mean difference⫾1 SD; if not available, the statistical test provided by the author is stated.
†RF (%)⫽(LVSV⫺RVSV)/LVSV⫻100.
‡RF (%)⫽(TSV⫺FSV)/TSV⫻100.
§Interobserver reproducibility.
㛳Intraobserver reproducibility.
¶RF (%)⫽(LVSV⫺RVSV)/LVSV⫻100.
#RF (%)⫽(LVSV⫺RVSV)/LVSV⫻100.
**Mean variation in RVSV and LVSV.
††RVindex⫽TSVindex⫺FSVindex; RF⫽RVindex/TSVindex.
‡‡RV⫽TSV⫺FSV; RF⫽RV/TSV.

transesophageal echocardiography than does gradient echo
cine imaging.31 Some of these studies have included patients
with bicuspid aortic valves. Planimetry, however, is a less
than optimal approach in patients with calcific stenosis. This
is because leaflet calcification and jet turbulence can make
accurate visualization of the true orifice difficult and
because of the complex, 3-dimensional shape of the
stenotic orifice. Tomographic measurements assume a
planar orifice that lies entirely within the image plane. In
addition, physiological valve area, which correlates better
with clinical outcome, is smaller than anatomic valve area
owing to contraction of the flow stream as it passes
through the narrowed orifice.38
Few data are available comparing physiological (conti-
nuity equation) valve area between CMR and echocardi-
ography, although this approach is feasible on the basis of
CMR velocity mapping of the velocity-time integral in the
left ventricular outflow tract and aortic valve orifice.26 The
different concepts underlying anatomic and physiological
valve areas may explain some of the apparent discrepan-
cies in comparisons of diagnostic approaches. These com-
parisons are most appropriate when measurements based
on similar concepts are compared (Tables 2 and 3).23–37
For evaluation of mitral stenosis, 2 methods are commonly
used to determine valve area: planimetry and pressure half-
time.39 A trend can be identified for CMR to overestimate the
 Cawley et al
pressure half-time valve area compared with echocardiogra-
phy; however, a close correlation is seen between CMR and
echocardiographic planimetered valve areas (Table 3).23,32–37
Planimetry of the mitral valve is a well-validated echocardio-
graphic approach, because anatomy of the stenotic mitral
valve results in a planar elliptical orifice in diastole.39 To find
the minimal mitral or aortic valve orifice on CMR images,
thin (preferably 4 mm or less) overlapping slices are used as
opposed to the usual 6- to 8-mm slices used for ventricular
imaging. Reproducibility rates, as measured by interstudy,
interobserver, and intraobserver variability of CMR for both
aortic and mitral stenosis, are acceptable for clinical use
(Tables 2 and 3).23–37
Evaluation of Valve Regurgitation
CMR uses qualitative and quantitative indices of regurgitant
severity similar to echocardiography: regurgitant jet area,
regurgitant volume, and regurgitant fraction. Unlike stenosis
severity, regurgitant severity in the past typically has only
been clinically reported in qualitative or semiquantitative
ways. With the endorsement of the 2006 American College of
Cardiology/American Heart Association guidelines on valvu-
lar heart disease and the 2003 American Society of Echocar-
diography guidelines on valve regurgitation, clear recommen-
dations are now available on how to quantify valve
regurgitation.40 – 42
Regurgitant Jet Area
The presence of a regurgitant jet can be visualized with cine
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pulse sequences, either SSFP or gradient echo. Flow turbu-
lence across valves produces a loss of net signal (signal void)
on cine pulse sequences due to dephasing of protons43;
however, correlation of the degree of signal void with the
severity of regurgitation can be problematic, because the
appearance of the signal void is highly dependent on pulse-
sequence parameters.7,43,44 Early studies using CMR to eval-
uate valve regurgitation (aortic or mitral) focused on visual-
izing the signal void, with validations based on qualitative
assessment or measurement of jet length or area compared
with color Doppler or angiography (Tables 4 and 5).45,45–58
Evaluation of regurgitant severity based on jet area or length
is no longer recommended, because this method is not a
reliable indicator of disease severity. Nevertheless, visualiza-
tion of distal flow disturbance by CMR, echocardiography, or
angiography remains useful for detection of regurgitation and
evaluation of jet direction and origin. Quantitation now
focuses on proximal jet geometry, including vena contracta
width and regurgitant orifice area.
Regurgitant Volume and Fraction
Regurgitant volume is defined as the amount of blood that
flows in a retrograde direction across the valve with each
heartbeat. Regurgitant fraction is the regurgitant volume
expressed as a percentage of total stroke volume. CMR
allows calculation of regurgitant volume by calculating the
differences between right and left ventricular volumes, either
by cine assessment of ventricular volumes or by velocity
mapping and flow quantitation in the pulmonary artery and
aorta. In the absence of cardiac disease, right and left
CMR for Valve Disease: Technique and Validation 475
ventricular stroke volumes are equal. With valve regurgita-
tion, assuming only 1 valve is affected and no intracardiac
shunt is present, the difference in stroke volumes reflects the
regurgitant volume. Most adults with chronic valve regur-
gitation have significant regurgitation of only a single
valve, which makes this approach widely applicable (Ta-
bles 4 and 5).45–58
Phase contrast can directly quantify antegrade and retro-
grade flow volume across semilunar valves (Figures 4 and 5).
To evaluate aortic regurgitation, phase-contrast imaging is
performed in the aortic root, and total stroke volume and
regurgitant volume are measured directly as the antegrade
and retrograde transaortic volume flow rates.47–50 The same
approach can be used for the pulmonic valve. Phase-contrast
imaging of the mitral valve is more difficult because of the
movement of the mitral valve annulus during ventricular
systole. An alternative approach for measuring mitral regur-
gitation is to calculate total left ventricular stroke volume
with SSFP imaging and forward stroke volume in the aorta
using phase-contrast imaging. The difference between these 2
values represents the regurgitant volume. This technique is
useful because in patients without mitral regurgitation, for-
ward stroke volume has a very close correlation with total
stroke volume.10,13,14
Limited CMR studies on assessment of regurgitant orifice
area (mainly by planimetry with aortic regurgitation) are
available, even though this is 1 of the key variables in the
assessment of regurgitant severity and the strongest predictor
of clinical outcome.59,60 Planimetry of the aortic valve to
determine the regurgitant orifice area has the same problem
as does planimetry of the aortic valve for stenosis: The orifice
does not lie in a single plane, and contraction of blood flow
results in a smaller effective regurgitant orifice area than the
anatomic area.
Right-Sided Valve Disease
Pulmonary Valve Disease
Pulmonic valve regurgitation is a major late complication
after surgical repair of tetralogy of Fallot. Echocardiographic
evaluation of pulmonic regurgitation severity is largely qual-
itative, based on vena contracta width and the density and
deceleration slope of the continuous-wave Doppler signal. In
addition, 2D imaging of the pulmonic valve in adults can be
very challenging because of poor acoustic access. In the
clinical setting, assessment of right ventricular function is
only qualitative, because the complex shape of the right
ventricle limits simple approaches to calculation of volumes
and ejection fraction.
CMR provides visualization of the pulmonic valve and
regurgitant jet, quantitation of regurgitant severity, and accu-
rate measurement of right ventricular volumes and ejection
fraction. Quantitation of pulmonic regurgitation by phase
contrast has been validated against CMR right and left
ventricular stroke volumes.61 Other studies are primarily
limited to comparisons of quantitative CMR with qualitative
echocardiographic measures, although 1 study showed a close
correlation between regurgitant fraction by CMR and Dopp-
 476 Circulation January 27, 2009
ler pulmonary regurgitant severity defined by the diastolic
duration of regurgitant flow on continuous-wave Doppler.62
CMR allows accurate quantitation of right ventricular
volumes and ejection fraction because it allows direct visu-
alization of the right ventricle in multiple tomographic planes
and does not rely on geometric assumptions about chamber
shape. In adults with chronic pulmonic regurgitation after
tetralogy of Fallot repair, CMR has been used to measure the
reduction in right ventricular volumes after valve replace-
ment.63,64 One retrospective study suggested that right ven-
tricular volumes may be an indicator of the optimal timing of
pulmonic valve intervention.64 Prospective studies of this
promising approach to the timing of pulmonic valve inter-
vention are needed.
Tricuspid Valve Disease
Tricuspid regurgitation can be visualized on the basis of its
signal void with cine imaging. Phase-contrast imaging of the
tricuspid valve presents the same challenges as with the
mitral valve owing to annular motion with the cardiac cycle.
Tricuspid regurgitation can be calculated in terms of regur-
gitant volume and fraction in similar ways to mitral regurgi-
tation: The forward stroke volume, as measured in the
pulmonary artery with phase contrast, is subtracted from the
total right ventricular stroke volumes from the SSFP images.
Other Cardiac Imaging Approaches
Computed tomography can provide accurate anatomic images
of valves and valve motion. Computed tomography also
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provides precise quantitation of aortic valve calcification;
however, quantitation of valve hemodynamics is predomi-
nantly limited to planimetry methods (valve area for stenosis
and regurgitant orifice area for regurgitation).65– 68
Clinical Implications
The primary advantage of CMR for assessment of valvular
heart disease currently is its accurate and reproducible mea-
surement of biventricular volumes and function in adults with
chronic aortic, mitral, or pulmonic regurgitation. CMR may
also provide a quantitative measure of valve stenosis and
regurgitation, including regurgitant volume and fraction. As
interventions for valve disease improve and are recom-
mended earlier in the disease course, it becomes particularly
important to ensure that patients do in fact have severe valve
dysfunction and that our measures of ventricular size and
function are precise and accurate. CMR is a promising
approach for providing these data.
Despite the promise of CMR for evaluation of valve
disease, some limitations still exist. Notwithstanding many
published validation studies, these methods have not been
widely used, and clinical experience is limited. CMR has not
been shown to provide reliable information on pulmonary
artery pressures or regurgitant orifice area, data that echocar-
diography does provide. In addition, echocardiographic cri-
teria have been validated and compared with clinical out-
comes, data that are not yet available for CMR measures of
valve disease. Given the potential strengths of CMR, prospec-
tive studies using this approach to define disease progression
and the optimal timing of intervention are needed. CMR may
also provide a more accurate, precise, and reproducible
measure of disease severity for trials of medical therapy in
chronic valve disease.
Sources of Funding
Dr Cawley is supported in part by grants from the Society for
Cardiovascular Angiography and Interventions and General Electric,
as well as by the John L. Locke Jr Charitable Trust.
Disclosures
Dr Maki serves as a consultant and on the speakers’ bureau for
Bracco Diagnostics. The remaining authors report no conflicts.
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KEY WORDS: echocardiography 䡲 imaging 䡲 magnetic resonance imaging
䡲 regurgitation 䡲 rheumatic heart disease 䡲 valves